Hypothalamic resistin induces hepatic insulin resistance
J. Clin. Invest. Evan D. Muse, et al. 117:1670 doi:10.1172/JCI30440 [
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Figure 2Central resistin increased hepatic glucoses fluxes predominantly via glycogenolytic pathways. (
A and
B) icv or IH infusion of resistin (black bars) resulted in 2- to 3-fold increases in hepatic flux through G6Pase (
A) and glucose cycling (
B) compared with vehicle (white bars). (
C and
D) Increased hepatic glucose fluxes were mainly accounted for by an increased rate of glycogenolysis (
D) rather than gluconeogenesis (
C). (
E) Quantitative real-time RT-PCR revealed that central resistin had no effect on the hepatic expression of the key gluconeogenic enzymes PEPCK and G6Pase. (
F) Decreased levels of p-AMPKα were apparent in the livers of resistin-treated animals as analyzed by immunoblot. *
P < 0.05 compared with vehicle.
